The involvement of orexins and BDNF on behavioral consequences induced by caloric restriction

• Grant number: 13/06569-5
• Support type: Scholarships in Brazil - Doctorate
• Effective date (Start): September 01, 2013
• Effective date (End): March 31, 2017
• Field of knowledge: Biological Sciences - Pharmacology - Neuropsychopharmacology
• Principal researcher: Sâmia Regiane Lourenço Joca
• Grantee: Laura Alves Stanquini
• Home Institution: Faculdade de Ciências Farmacêuticas de Ribeirão Preto (FCFRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

BDNF is a neurotrophin with a high level of expression in the Central Nervous System (CNS). This neurotrophin acts binding in the receptor TrkB and can facilitates the neuronal survival and differentiation. BDNF also seems to play a key role in energy homeostasis since haploinsufficiency of BDNF or its receptor TrkB leads to excessive early weight gain and hyperphagia. Several lines of evidence have pointed that caloric restriction can modulate the signaling of BDNF in limbic structures of the CNS. Furthermore, caloric restriction alters several signaling factors responsible for the control of energy homeostasis, including the increased release of peptides orexins A and B (OXA and OXB, respectively), at lateral hypothalamus. The orexins-releasing neurons project to several areas of the CNS such as the hippocampus and cortex. Moreover studies suggest that the expression of OXA modulates the behavior of adaptive responses to stress, and this effect can be mediated by facilitation signaling of BDNF. Thus, evidence suggests that caloric restriction promotes an antidepressant-like effect that would be promoted by increased release of OXA. Moreover, studies indicate that signaling OXA increased by food restriction lead to behavioral effects by increasing the expression of BDNF.Therefore, the hypothesis of this work is that the antidepressant effect of caloric restriction is being mediated by an increase in OXA in the hippocampus and / or cortex, which bind to OX1R receptors and facilitates the BDNF signaling, with the activation of TrkB.

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

STANQUINI, LAURA A.; RESSTEL, LEONARDO B. M.; CORREA, FERNANDO M. A.; JOCA, SAMIA R. L.; SCOPINHO, AMERICA A. Prelimbic cortex 5-HT1A and 5-HT2C receptors are involved in the hypophagic effects caused by fluoxetine in fasted rats. Pharmacology Biochemistry and Behavior, v. 136, p. 31-38, SEP 2015. Web of Science Citations: 3.